| First Author | Kandil O | Year | 1988 |
| Journal | Brain Behav Immun | Volume | 2 |
| Issue | 1 | Pages | 32-49 |
| PubMed ID | 3263157 | Mgi Jnum | J:26026 |
| Mgi Id | MGI:73752 | Doi | 10.1016/0889-1591(88)90004-9 |
| Citation | Kandil O, et al. (1988) Stress-induced decline in immune responsiveness in C3H/HeJ mice: relation to endocrine alterations and tumor growth. Brain Behav Immun 2(1):32-49 |
| abstractText | We examined the effect of rotation-induced stress on (1) growth of lymphosarcoma tumors; (2) interleukin-2 (IL-2) production; (3) T cell subset distribution; and (4) cytotoxic T cell (CTL) function. In addition, we examined the levels of corticosterone and beta-endorphin as possible mediators of stress-induced immune alterations. Rotation stress induced progressive lymphosarcoma growth, while unstressed mice showed tumor regression after 2 weeks of growth. IL-2 production and CTL activity in stressed animals were significantly lower than controls during the first 2 weeks after initiation of stress. Spleen lymphocytes from stressed and control mice bearing the L3T4 antigen (helper/inducer T cell marker) remained unchanged, while in peripheral blood such cells decreased in stressed but not control animals. This latter pattern was also observed in Lyt 2 positive (suppressor/cytotoxic) cells of both spleen and peripheral blood. Corticosterone levels were elevated for an extended period following initiation of stress, while beta-endorphin levels remained similar to those of the controls. Although these data do not directly establish a causal link between immunoinhibition and tumor growth, they clearly demonstrate that stress inhibits a number of cell-mediated immune functions that may be relevant in this regard. |
